Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.4.23.15 (renin)
 35,795 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The distribution of renin was investigated by immunofluorescence in human kidney biopsy specimens (27 patients with lipoid nephrosis, 39 with Berger disease, 17 with membranous glomerulonephritis, 5 with thrombotic microangiopathy, and 7 with malignant nephroangiosclerosis). A semiquantitative assessment was carried out. Two ratios were found significatively increased in the study groups as compared with the control group: JGA + and JGA ++ which expressed, respectively, the number of fluorescent JGA in relation to the number of glomerular sections and the number of fluorescent JGA with more than six renin-containing cells (RCC) in relation to the number of immunoreactive JGA. Highest values were observed in patients with thrombotic microangiopathy and malignant nephroangiosclerosis (P less than 0.001). The above immunomorphological parameters were correlated with clinical and laboratory data. A positive dependency was found between JGA + and JGA ++ ratios and a low sodium diet, diuretic therapy and serum creatinine. A negative dependency was seen in the albumin and hemoglobin serum levels. No correlation was found with blood pressure values. These observations suggested that decreased plasma volume and impaired renal function could be factors leading to an increased renin production in the kidney.
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PMID:Abnormalities of renin-containing cells in human glomerular and vascular renal diseases. 634 85

In order to explore immunological features of hypertension, we studied autologous immune complex nephritis (Heymann nephritis) combined with DOCA-NaCl treatment. This combination resulted in hypertension and increased heart weight whereas DOCA-NaCl treatment alone induced only a slight elevation of blood pressure and a moderate increase in heart weight. Nephritic rats without DOCA-NaCl load remained normotensive, their heart weights being comparable to those of controls. This new model of hypertension was neither characterized by azotemia nor by reduced renal excretory capacity. Hypertension was not renin-angiotensin-dependent. DOCA-NaCl treatment accelerated the development of proteinuria. In the hypertensive rats, systolic blood pressure to daily urinary protein excretion. Renal histopathology revealed changes resembling those of malignant nephrosclerosis. Immunohistology and electron microscopy showed a typical membranous glomerulonephritis in all immunized animals. It was concluded that immune complex disease of the Heymann nephritis type may interfere with normal hemodynamic adaptation to hypervolemic sodium load, resulting in hypertension.
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PMID:Autologous immune complex nephritis and DOCA-NaCl load: a new model of hypertension. 644 27

The binding of antibodies to podocytic antigens such as the Heymann antigen or aminopeptidase A may lead to the induction of a membranous glomerulonephritis in several species. To study the possible future interactions of antibodies with antigens on these podocytes, epithelial cells from isolated mouse glomeruli were cultured. By indirect immunofluorescence, the cells were positive for cytokeratin, vimentin, desmin, and the ZO-1 protein, a component of the tight junction complex. When rat monoclonal antibodies were used, the cells were also positive for the hydrolases aminopeptidase A and dipeptidyl peptidase IV, and they stained with ASD-33, a monoclonal antibody that recognized an epitope only present on the cell membranes of mouse podocytes. They were negative for the von Willebrand factor and did not stain with a monoclonal antibody (ASD-13) that binds to endothelial cells of glomeruli and peritubular capillaries. By electron microscopy, the cells showed tight junctions but lacked Weibel Palade bodies (endothelium), desmosomes, and cilia (parietal epithelium). The mRNA expression of several components of the renin-angiotensin system was also examined, and some factors indirectly coupled to the renin-angiotensin system component angiotensin II in this podocytic culture by RT-PCR analysis. mRNA Expression for the angiotensin II degrading hydrolase aminopeptidase A and angiotensinogen was found, but this was not found for any other component of this system, such as renin, angiotensin-converting enzyme, or the angiotensin II receptors AT1a, AT1b, and AT2. Low mRNA expression for dipeptidyl peptidase IV was observed. In addition, expression of the growth factors transforming growth factor-beta and interleukin-7, and the extracellular matrix components fibronectin, laminin B2, perlecan, and collagen IV alpha 1, was observed. Given these characteristics, a glomerular epithelial cell culture with features of podocytes in vivo that will allow future studies on the interaction of anti-aminopeptidase A monoclonal antibodies and angiotensin II with aminopeptidase A was established. This is of interest in light of the observation that injection of mice with anti-aminopeptidase A antibodies causes an acute albuminuria.
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PMID:Mouse glomerular epithelial cells in culture with features of podocytes in vivo express aminopeptidase A and angiotensinogen but not other components of the renin-angiotensin system. 917 40

We investigated the hemodynamic, renal, and hormonal effects of cyclosporin A (CyA) treatment (6 mg/kg per day) for 4 weeks in 12 patients with nephrotic syndrome (8 women: 4 men, aged 36-66 years, 3 cases of focal glomerular sclerosis: 9 cases of membranous nephropathy). To evaluate the effects of CyA on the diurnal variation of blood pressure (BP), 24-h non-invasive BP monitoring was performed using model ABPM-630 (Nihon Colin, Tokyo, Japan) before and during CyA treatment. As indices of hemodynamics, intra-arterial pressure was monitored and cardiac output was measured by the dye-dilution technique using a cuvette at 0 and 4 weeks after treatment. CyA ameliorated urinary protein excretion and hypoproteinemia from 3.5 +/- 0.9 to 2.2 +/- 0.7 g/day, and serum protein concentration from 4.9 +/- 0.2 to 5.5 +/- 0.2 g/dl after 4 weeks' treatment. Endogenous creatinine clearance, 24-h urinary sodium excretion, and plasma renin activity decreased significantly at 1 week. CyA treatment raised casual BP from 122 +/- 4/75 +/- 2 to 140 +/- 5/87 +/- 3 mmHg after 1 week and to 146 +/- 4/90 +/- 2 mmHg after 4 weeks. Before treatment 24-h ambulatory BP monitoring showed BP reduction at night (116 +/- 5/68 +/- 3 mmHg) compared to the daytime (124 +/- 5/75 +/- 2 mmHg). The diurnal variation of BP disappeared during CyA treatment; mean daytime and nighttime pressures were 135 +/- 4/81 +/- 2, 132 +/- 5/80 +/- 3 mmHg at 1 week and 139 +/- 5/83 +/- 3, 131 +/- 6/80 +/- 3 mmHg at 4 weeks, respectively. On hemodynamic study; a 4-week treatment with CyA increased mean arterial pressure from 91 +/- 3 to 104 +/- 3 mmHg, total peripheral resistance index from 2.1 +/- 0.1 to 2.5 +/- 0.1 x 10(3) dyne.sec.cm-5.m2, and unchanged heart rate and cardiac index. Serum Mg concentration decreased from 2.1 +/- 0.1 to 1.7 +/- 0.1 mg/dl. These results suggest that CyA-induced hypertension is characterized by the loss of nocturnal decline in blood pressure, which is accompanied by volume retention after 1 week and systemic vasoconstriction after 4 weeks.
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PMID:[Effects of cyclosporin A on the diurnal variation of blood pressure in patients with nephrotic syndrome]. 919 62

Five nephrotic patients, who did not present sodium retention when on sodium balance, have been studied. All had membranous nephropathy, were normotensive and renal function was normal in 2 and slightly reduced in 3. The following parameters were measured: 24-hour excretion of aldosterone, the response of plasma renin activity (PRA) and of plasma aldosterone to upright posture, postural changes of the fractional excretion of sodium and lithium, and natriuretic response to spironolactone. The resting values of plasma aldosterone were low in all patients, and after stimulation by upright posture they increased hardly to the low-normal limit only in 1 patient. Resting PRA was normal in all patients and increased slightly, after stimulation. The 24-hour urinary excretion of aldosterone was low in 4 patients and borderline in 1. No natriuretic response to spironolactone was observed in any patients. After upright posture the fractional excretions of sodium and lithium decreased significantly and to the same extent in all patients. Four nephrotic patients with fluctuating, spontaneous episodes of sodium retention and of sodium excretion have been studied as controls. These patients had normal values of urinary aldosterone and of resting PRA and aldosterone. After upright posture the changes of PRA and of aldosterone were clearly evident in 2, and exaggerated in the other 2 patients. In these patients, a significant increase of sodium excretion occurred after treatment with spironolactone. These results suggest that a not negligible number of patients with nephrotic syndrome have hyporeninemic hypoaldosteronism. This diagnosis should be taken into account when investigating the role of aldosterone in sodium retention in nephrotic syndrome.
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PMID:Hyporeninemic hypoaldosteronism in patients with nephrotic syndrome. 962 45

Several studies in patients with chronic kidney diseases have shown that men have a more rapid disease progression than women. Also, with ageing, men exhibit greater decrements in renal function and increased glomerular sclerosis than women. Data from meta-analysis studies indicate that women with several non-diabetic renal diseases such as membranous nephropathy, IgA nephropathy and polycystic kidney disease present a slower progression, but in diabetic renal disease this is not yet established. Thus, men appear to be at greater risk for renal injury than are women, but the underlying mechanisms are unknown. Sex hormones may mediate the effects of gender on chronic renal disease, through the interaction with the renin-angiotensin system, the modulation of nitric oxide synthesis and the downregulation of collagen degradation. New observations indicate that androgens may contribute to continuous loss of kidney cells though the stimulation of apoptotic pathways. Apoptosis is an unique type of programmed cell death which is activated in several chronic kidney diseases. Studies in vitro indicate that androgens prime a Fas/FasL dependent apoptotic pathway in kidney tubule cells. This apoptotic cell death pathway is receptor-linked and interacts with the mitochondrial pathway, which may be activated by other mechanisms, such as toxins and ischemia. Therefore, the mechanisms to cell death which are primed by androgens may interact with others occurring in several conditions leading to the loss of renal cells. These findings are consistent with a role for androgens to promote chronic renal injury in men.
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PMID:Gender and the progression of chronic renal diseases: does apoptosis make the difference? 1519 27

A 77-year-old man with membranous nephropathy was treated with triple blockade of the renin-angiotensin-aldosterone system and developed subileus six times in 5 months. The resection of his sigmoid colon uncovered angioedema. It should be noted that angiotensin-converting enzyme or angiotensin receptor blocker can cause angioedema of the intestine and induce subileus.
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PMID:Repeated subileus due to angioedema during renin-angiotensin system blockade. 1684 40

Nonsteroidal antiinflammatory drugs (NSAIDs) have potentially important renal adverse effects. With regard to renal adverse effects there is no indication of significant differences between conventional NSAIDs and selective COX-2 inhibitors. Their nephrotoxicity has been well documented. Many of the renal abnormalities that are encountered as a result of NSAIDs use can be attributed to the inhibition of prostaglandins synthesis. The release of prostaglandins is particulary importent in high-risk patients, including patients with severe heart disease, liver disease, preexisting renal disease, elderly and patients with volume depletion. The common complication of NSAID use is retention of sodium and edema formation due to increased reabsorption of sodium and water in the loop of Henle and hyperkalemie due to diminished renin secretion. Nonsteroidal antiiflammatory drugs can induce two different forms of acute renal failure. Decreased prostaglandin synthesis can lead to reversible renal ischemia and hemodynamically-mediated acute renal failure. Second form of acute renal failure is acute interstitial nephritis. This type of interstitial nephritis is often accompanied by nephrotic syndrome due to minimal change disease. Nephrotic syndrome after NSAIDs treatments may be also associated with membranous nephropathy. Another complication of NSAIDs treatment is modest rise of systemic blood pressure in some hypertensive patients due to increase in renal and systemic vascular resistence. In patients consuming excessive amount of NSAIDs over a prolonged period of years papillary necrosis can occur. Exposure to large quantities of NSAIDs can probably induce in some patients chronic renal insufficiency.
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PMID:[Nonsteroidal antiinflammatory drugs and the kidney]. 1696 9

The mechanisms of hypertensive nephrosclerosis are not fully understood. In experimental models of the disease, inflammatory reactions such as macrophage infiltration play an important role. In human hypertensive nephrosclerosis, however, there have been few studies examining the role of inflammation histologically. We investigated whether the number of infiltrating macrophages was increased in human hypertensive nephrosclerosis, and evaluated the effects of a blockade of the renin-angiotensin system on clinical and histological findings. We examined macrophage infiltration using immunohistochemistry in renal biopsy specimens obtained from 16 patients with hypertensive nephrosclerosis, 5 patients with IgA nephropathy, 5 patients with membranous nephropathy, and 5 patients with minimal change nephrotic syndrome. The number of infiltrating macrophages in glomeruli was significantly larger in the patients with hypertensive nephrosclerosis than in those with minimal change nephrotic syndrome. The patients with hypertensive nephrosclerosis were divided into groups based on their use of antihypertensive agents at the time of renal biopsy. We investigated the effects of antihypertensive agents on clinical findings, macrophage infiltration, and monocyte chemoattractant protein-1 expression. There was no difference in clinical findings between the hypertensive groups. The numbers of infiltrating macrophages and monocyte chemoattractant protein-1-positive cells in glomeruli were significantly smaller in patients treated with an angiotensin-converting enzyme inhibitor or angiotensin II type 1 receptor blocker, whereas calcium channel blockers had no influence on histological findings. In conclusion, inflammation is involved in the progression of human hypertensive nephrosclerosis and the inflammatory process is inhibited by blocking the renin-angiotensin system.
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PMID:Effects of renin-angiotensin system blockade on macrophage infiltration in patients with hypertensive nephrosclerosis. 1778 32

Renal disease is a major cause of mortality and morbidity in systemic lupus erythematosus. Among the histological classes of lupus nephritis, membranous nephropathy comprises only one-fifth of all cases. Reported survival and rates of end-stage renal disease in membranous lupus nephropathy (MLN) vary considerably, because of substantial heterogeneity among the published studies. The risk of progression from MLN to renal failure is generally reduced in the absence of proliferative lesions, but patients are, nevertheless, at risk of thromboembolic complications. The optimal therapy for MLN remains elusive because of a lack of controlled trials; however, cardiovascular protection and blockade of the renin-angiotensin system should be instituted early in all patients. Mixed membranous and proliferative lupus nephritis should be treated in the same way as pure proliferative lupus nephritis. If MLN is not accompanied by proliferative lesions but is associated with clinically relevant proteinuria, renal insufficiency or failure to respond to supportive therapies, immunosuppressive treatment is indicated. Treatment options include glucocorticoids combined with azathioprine, calcineurin inhibitors or alkylating agents. The efficacy of mycophenolate mofetil in MLN remains to be confirmed. Controlled trials to compare existing immunosuppressive agents and experimental modalities such as sirolimus, rituximab and infliximab should be undertaken in the future.
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PMID:Membranous nephropathy in systemic lupus erythematosus: a therapeutic enigma. 1932 86


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